Obesity-associated inflammation induces molecular stress responses in porcine fallopian tube and ovarian surface epithelium.

Chronic low-grade inflammation associated with obesity is increasingly recognized as a modifier of epithelial homeostasis within the female reproductive system. However, its early molecular consequences in physiologically relevant large-animal models remain insufficiently defined. To examine whether obesity-linked systemic inflammation is accompanied by alterations in epithelial stress markers in the Fallopian tube and ovarian surface epithelium of slaughterhouse-derived sows. Animals were retrospectively classified into lean (75-100 kg, n=3) and obese (200-250 kg, n=3) groups based on post-mortem body weight and circulating inflammatory markers. Plasma concentrations of CRP, IL-6, IL-1β, and TNF-α were measured <i>via</i> ELISA. <i>TP53</i> and <i>PAX8</i> transcript abundance was assessed using RT-qPCR, while protein levels and localization were evaluated by Western blotting and immunofluorescence. Obese sows exhibited elevated plasma CRP (+22.9%, p<0.05), IL-6 (+85.7%, p<0.05), and IL-1β (+140.2%, p<0.01), alongside a marked decrease in TNF-α (-73.1%, p<0.001), confirming a distinct inflammatory profile. <i>TP53</i> mRNA levels were higher in both the Fallopian tube and ovarian cortex, whereas <i>PAX8</i> expression showed a trend toward reduction in the Fallopian tube, although without statistical significance. Western blotting revealed significantly increased p53 protein levels in the Fallopian tube (p<0.05). Immunofluorescence demonstrated enhanced p53 and PAX8 signals in the Fallopian tube epithelium (p<0.01 and p<0.001, respectively), and a focal increase in p53 abundance in the ovarian surface epithelium (p<0.01). Concluding, obesity-associated inflammation is accompanied by molecular stress signatures in porcine reproductive epithelia, particularly within the Fallopian tube. Although these alterations should not be interpreted as preneoplastic, they may represent early adaptive or dysregulated responses to chronic metabolic burden, warranting further validation in larger cohorts.